PeriPheral Vestibular and Cerebellum disorders with ......with aPPliCations (module Four) transcript – review of Key Concepts Presentation by drs. datis Kharrazian and brandon brock

MODULE FOUR TRANSCRIPT: REVIEW OF CONCEPTS | COPyRIghT © 2016 FUNCTIONAL NEUROLOgy SEMINARS LP | PAgE 1

PeriPheral Vestibular and Cerebellum disorders with aPPliCations (module Four)

transcript – review of Key Concepts

Presentation by drs. datis Kharrazian and brandon brock

dr. Kharrazian

Well, everyone, thank you for coming to or attending or streaming the vestibular program, vestibular and cerebellum. We have this module set up for… The vestibular and cerebellar system are very integrated. So what we really focus on in this section is the peripheral vestibular system and peripheral vestibular disorders, with a little bit of integration into the cerebellum and the aspects of the cortex. In the next section we’ll really dive into more of the cerebellar integration.

So, the most important thing really isn’t just to learn information, but it’s really to understand the clinical thought process and how to diff-di some of these things.

So, do you want to mention a few things?

dr. brock

Yeah. With the peripheral vestibular system, it’s kind of like the cornerstone of learning neurology to a certain extent, because you really learn the difference between what’s happening sort of outside the skull and what’s happening inside of the skull, and all those receptors that are in the vestibular apparatus. So we take a lot of pride in not passing this section over and assuming that everybody learned it in school. What we found is, is that the vestibular anatomy wasn’t learned maybe all that well, and then taking that anatomy and the physiology, and turning it into a clinical picture, and then beyond that, the ability to differentially diagnose that clinical picture is just something that I think we need to review really well, especially as we go into the next module, which is central vestibular pathology, and then the module after that, which is mainly ocular function and pathology.

And really, the next three modules all bundle together into one big picture, so you can weave in and out of what’s going on with somebody if they walk in and fill out that they’re unstable, or they have dizziness, or they have a pathology that is considered vertiginous. So it’s an exciting, really, three-series stretch. It’s almost like three modules that are within one group themselves. So, we’re enjoying it.


dr. Kharrazian

Okay, so one of the things just to really kind of point out there is, most practitioners, most doctors, most alternative health care practitioners, they have no idea what to do with dizziness. They really don’t. The person who’s dizzy walks into a conventional medicine model, they usually will be just prescribed anti-nausea types of medications, and even medications that deal with the symptoms, but there’s no actual treatment. Some of them may get referred to a specialist. Just so you guys know, in San Diego, there’s two otoneurologists, neuro… neurologists. That’s it. And they have huge waiting lists, and, you know, they’re not… You know, I think they’re okay. But the point is, is that there’s many people that have dizziness really don’t know where to go. And dizziness can be so easy to treat sometimes when it’s as simple as BPPV, that no one knows how to do anything for, or very few people know how to train with it. But the actual patient that’s dizzy, if you see that they have dizziness, they usually learn to live with it, and they kind of adapted to it, unless it’s acute and then they freak out and they need to get proper attention. But for the most part, people that have recurring dizziness, or chronic dizziness, they really have nowhere to go. And if you really understand this skill well, you’ll be able to help a lot of people that are out there.

So, master dizziness, and then you… And you should always small. You know this information, someone walks into your office, their chief complaint is dizziness, you should just smile. You go, “I know exactly how to work this up. I know how to rule out everything, rule in everything, and I know how to treat it.” Alright? So that’s the level of confidence you want to have. Someone walks in, chief complaint dizziness, you want to smile. Right? If you don’t smile, and you freak out, it means you don’t have a thinking, clinical thought process, right? And then maybe something you do will help the dizziness. But if you do that, more than half the time you’ll probably make them much worse. So if you don’t know how to treat dizziness, and you just go in there and you start treating them, you might make them worse. Alright? So just randomly do acupuncture, or randomly do manipulation, or just to throw out some anti-nausea medication, is really not a good approach, alright?

dr. brock

Especially if it’s peripheral vestibular. You’re going to find, at the end of the weekend, this is probably the easiest section of everything we’ve taught. I’m hoping. And really, we, again, made an intake form for you that has not just a vestibular intake section, but it has questions related to each condition. So the neuronitis section has questions, the BPPV section has questions, the fistula section has questions. So really, that… Vestibular disorders are probably, depending on how good you are, sixty to seventy to maybe eighty percent subjective. Do you know how to ask the right questions? Well, we just made it for you.

So, I put that in the presentation. I want you to understand, we put that in kind of at the last minute as far as putting it in the slides, so it’s not in your notes, but you have the forms. So don’t worry about it not being on a slide. You have it. I know people get frantic when there’s a slide that doesn’t look like one that I have, but it’s just… I just broke it into pieces for you, that’s all. Just to teach it. But anyway, we’re going to have a great weekend. It’s going to be very systematic, it’s going to be very linear, it’s going to build. We’re going to review some old concepts, jump into new concepts, and tomorrow it’s pretty much all demonstration of the maneuvers. We’re actually going to do them on stage, and they’ll be on video, so you guys will have them and be able to watch them again. Does that sound good? Okay.

So, take it away Dr. Kharrazian.


dr. Kharrazian

So, just one of the key things when you look at the vestibular system, when you look at neurology itself, it’s very linear. I mean, I’ve got to be honest with you. Because neurology is probably one of the easiest topics to learn. It really is. I mean, there’s a mass of information, right? But it’s, like, so linear. I mean, symptoms are so clear for certain patterns. So if you go through a history, and you find out if they see the world moving, or if they’re moving, or if it’s worse in dark or light, or if it’s acute, or if it’s recurring or chronic, you can narrow down your list so quickly. Right? So that’s the linear model. Whereas, you look at something like immunology, there’s nothing linear about it. It’s like, three-dimensional, and it’s going all over the place, there’s exceptions to the rules, and it’s a whole different ball game, alright? But when you look at neurology, I mean, it’s just… I think I always loved neurology because it was just so, like, ahh, so secure. You have this, and you have this, and it’s linear, and you can figure out these things.

So, when you look at the vestibular system, it’s really the same thing. So one of the things that I want to do first, though, is I want to review concepts of all the things that we’ve gone through so far, and then kind of blend it in to the vestibular system, and then have you guys, you know, understand these things.

The key thing as a clinician is, you understand key points from the history, right? Those are the questions you ask from your history, whether… Do you have spasticity or not? If they have spasticity, you know what? It’s probably an upper motor neuron or cortical involvement, right? Do you have hypotonia? Do you have dizziness? Do you have hyperkinetic movements? Do you have slowness of movement? So I think, as we’ve going through, and we’ve gone through every region of the brain, you realize there’s a pattern for each region of the brain, right? There’s a symptomology. There’s a clinical finding for each part of the brain.

So in the vestibular system, it’s the same way. There are symptoms that are involved, nystagmus being one of the key findings if the vestibular system’s firing; the direction it’s going in; the fast phase, the slow phase. Is it rotational? Is it a downbeat nystagmus? Is it an upbeat, right? Is it going to the right? It’s going to the left? Those all make it really, really clear and linear to know what area’s involved, right? And once you know what area’s involved, you can go in there and do appropriate treatment.

So, one of the key things that we’re trying to do in this program is, we’re trying to put together the concepts of: How do you merge and integrate? How do you look at metabolic issues? How do you look at neurological issues? Right? Because one of the problems we have in the general healthcare model is, we have specialties driven up, where you have a gastroenterologist, and a neurologist, and an internist, and then a family physician refers to each one of these specialists. But they’re all localized. But when you look at the brain, the brain gets impacted by hormones. It’s impacted by inflammation. It’s impacted by infections. It’s impacted by autoimmunity. Right? It’s impacted by things like diabetes. It’s impacted by blood flow and circulation. So to ignore all those things just means you’re not doing a thorough, complete job.

So, as we even go into this peripheral vestibular system, we’re going to spend a lot of time going into the metabolic factors and how they integrate, and then the question that comes up, once you have a complete picture, is: Do you do both at the same time? Do you do… Do you just do therapy for a while? Or do you do a nutritional, dietary approach to get their neuron endurance and their brain healthier? Right? Or do you go and do both together? When it comes to the vestibular system, and it’s a peripheral vestibular disorder, and dizziness and so forth, if you make the wrong call, your patient gets worse. If you have someone that’s


completely unstable, and then even though you make the right diagnosis and you start to treat them, they’ll just get dizzier. Right? And they’re worse off. If you can stabilize someone, and then do approaches that can be useful.

So, what I’m going to show you is, I’m going to show you just random clips of examination findings, and then I want you to just think about what region of the brain is involved. Right? Because it’s part of the skill of understanding how to work the patient. You see a clinical exam finding, you go, “There’s only so many things that could be, and if I see that, I need to check this, this, and this, and this is going to tell me where I need to go,” and then we went to different flow charts. One of the flow charts is, then you do repeat testing, and then look at their endurance and their metabolic capacity and so forth.

So, here’s a patient… I’m going to play this video here. So, first of all, what do you see with her right away? What is she doing? She’s looking down, she’s leaning forward, and she’s holding someone’s hand. So what does that tell you about her stability? It’s off. Now, the question you want to ask is, you know that her balance is off. Is she… What are some things you want to ask? Does she sway to one side? Does she veer to one side? Does she veer to the other side? Do you see truncal movement when she walks? Do you see head position in one angle when she’s walking versus another? So, if her head is positioned one way, what does that tell you? Maybe she’s recruiting a vestibular system, right? Could be that she’s deficient in one, and trying to work to the other, or it could just be that she’s falling because she’s lost her tone there.

[10.09]

So we always look, when we see dizziness, when we see people that we have imbalance and dizziness, and we have them… watch them walk, we always want to look at where their head positions are, right? If they’re down, and looking at the ground, you know they’re really unstable. So that’s the first thing. Then if you see some people that have, like, forward translation, you think of maybe things like the otoliths, if you see rotation, then you might see some vestibular canal compensation, right? So you’re looking at those head positions to see where they are. Some people will walk like this, like the otoliths, they’re unstable. So as you put them forward, they’ll just fall. So you’ll see all these different types of sways, which give you clues to what’s happening with their balance.

So just think of it this way: You have vestibular apparatus, you have canals, and we’ll go over these in more detail, right? So if you see head position, head rotation, you may think they’re trying to recruit a canal, right? Doesn’t mean they all are; it just means you have to consider that possibility. And then if you see translation of the head forward, or you see translation of the head back, you want to see, are they activating their sac… or their utricles? Do they have any otolith type of compensation, or deficits they’re trying to deal with? So looking at head posture is really very critical.

For the most part, if they are really bad, first thing they’ll do is look at the ground. So the minute you see someone look at the ground, you’re going, “This is a whole different ballgame.” They are very, very, very unstable, okay?

And then you want to look at their gait. Obviously if they have balance issues, what are you going to see with their stance? It’s going to be a wide stance, right? So you want to see… and the degree of how wide their stance is gives you a clue. And then you want to see them walk. And as they walk, you want to see


if what? They sway to one side or the other. They’re going to basically have… They have sway to the side where they’re falling, right? Lack of integration, lack of tone and recognition. And then as you look at their gait, you also want to see, do they have titubations? Are they shaking and moving as they’re walking? Which could be more like a truncal ataxia, which could be more cerebellar.

So those are the key, like, things to think about the minute you’re trying to evaluate a patient. Things like, for example, we went through this, we talked about things to look through. So let’s watch it. You guys tell me what you guys think could be involved. We know she’s unstable.

[unintelligible] “Yeah” [unintelligible]

Okay. Lots of things to dissect there, okay? Again, the key thing is, you have the clinical thought process as you go through stuff. So one of the things that you first see… What was your degree… How would you rate her degree of stability? Like, zero to a ten? It’s pretty bad, right? It’s to the point she’s got to hold her hand, and she’s all over the place. Do you notice how she’s also having difficulty feeling where the… like, she’s kind of not knowing where her feet are? So the minute you see that she doesn’t know where her feet are, or where things are, you have to consider the possibility: does she have a peripheral nerve issue? Right? Does she have a… let’s say, is she diabetic? Does she have her proprioceptive fibers, her large-diameter fibers, involved? Right? So that’s the first thing. Any time you see… any time you have slap, someone can’t feel the ground, and they’re just kind of stomping to try to get to the ground, they can’t judge where the ground is, or you see someone walking cautiously, and they don’t know where things are, they’re moving very slowly. So as you do a vestibular workup, you’ve got to make sure you don’t miss anything.

So the minute you see someone having issues with foot stomping, or putting their foot all over the place, you’ve got to pull out your vibration sense, your tuning fork, and boom, and then check vibration sense to see what’s going on. When you check vibration sense, remember that, you know, you can have people that just don’t recognize vibration, so you put it on their feet, and you see the vibrating and you ask them when it stops, first of all, if they can recognize vibration. But remember that there’s more vibration perception in the feet than there are in the shins. So what if you have someone that… So if you took a tuning fork right now, and hit it, and there’s vibrating, and you put it on your foot, on your toes on your foot, and then you put it on your shin, where would you feel more vibration? On the foot, because you have more proprioceptors – vibration sense receptors – there. What if they were equal? What does that tell you? Then they may have lost subtle vibration sense perception. Now, it could be peripheral nerve, could be parietal lobe – because these things integrate. Now, she could have a parietal lobe… not her, but in general. You see someone who’s cautious where they walk, they may have a parietal lobe issue. Because remember the parietal lobe is where you have involvement of where you are with visual… where your body is. Your brain has to recognize where your arm and feet and leg are. So when you see someone is unstable, don’t just jump into “it’s got to be the vestibular apparatus, and its…” you’ve got to go through and look at all the different variables. So when you see someone that cautious with her walking, you have to go and look at peripheral nerves, does she have anything going on with her parietal lobe, right? Those are some of the key things to think about.

Now, as she walked, did you guys see any head rotation? Any preference? Or was she just looking down? She’s just looking down. So she’s completely unstable, so she has to look down. Now, what did you notice about her spinal tone? And what did you notice about her motor control? Watch it one more time, okay?


She’s looking down. Really doesn’t know… Her feet are also very cautious. She has a hard time coordinating. What’s her truncal stability like? Terrible.

[unintelligible] “Yeah” [unintelligible]

So she’s got truncal instability, she’s got a little bit of truncal ataxia, she has a hard time coordinating and turning her foot on and off… So this is actually cerebellar disease. Which you don’t want to confuse cerebellar disease with a peripheral vestibular condition, right? So you see how her trunk was moving? See how she was unstable? So the cerebellum… Remember, the vestibulocerebellum, the cerebrocerebellum – right? – and spinocerebellum, they all have different types of presentations. You’re kind of seeing a mixture of these things with her. The fact that she’s lost her trunk stability – right? – that’s all spinocerebellum. And you know how people have dysdiadochokinesia, and they can’t coordinate muscles going on and off. You’re seeing that in her lower extremities. That’s the cerebrocerebellum that’s involved. So you’re seeing these mixed types of cerebellar issues, which then makes you start to think how you would rehab her and what things you would do.

Now, do you see a tendency for one side or the other? Sometimes hard to tell until you do individual side testing, but for the most part you should sometimes see bilaterality here, more than anything else. So this could be more of a degenerative, global cerebellar disease, or some type of genetic disorder. So those are things that you want to quickly go through, right?

So that’s just the clinical thought process. So, you see gait, you see their head position. So, let’s review one more time, then I’ll move on to the next time. So, when you’re looking at… We’re going to focus this weekend really on narrowing down into the vestibular system and dizziness patients and so forth like that, right? So when you’re seeing who’s unstable, and they come in to you and say their balance is off, they’re having vertigo and dizziness, as they move and as they ambulate you want to go and look at what’s going on. Start looking at head position. If they’re really bad, they have to look at the ground, okay? Now, then you want to see… Some people may recruit as compensation. They may look up to get more stable as they’re trying to walk and they’re starting to fall. They may look to one side. That means they’re trying to recruit one of their canals, right? That can help them become more stable, that gives you a clue that probably the opposite canal is involved, okay? Then look to see if they sway to one side, look at their wide-stance gait, see if they have any truncal movements, then see how their foot drop is, and if they’re hitting the ground hard, or if they can feel the ground. Those are all going to kind of let you know where you need to go. Anytime someone has instability, you start with their peripheral nerves, right? You work your way up through the proprioceptive large diameter fibers, you go up into the parietal lobe, you look at the cerebellum, and then you look at each of the vestibular canals and vestibular systems.

Let’s do another case. Okay. So, she’s going to basically do a Romberg, and then, and just… When you see a Romberg, you want to just, first of all, ask the question: if she’s stable, or if she’s swaying all over the place. And if she sways, does she have a tendency to sway in one region? Because wherever she sways can give you a clue which canal’s going to be more involved. Okay? And which cerebellum may be involved. So.

So are you guys noticing a sway, more on one side than the other? Now she increases her stance width, so she has more stability.


Okay. So if you had to guess which side of the vestibulocerebellar system is off, would you think left or right? Left, because she’s obviously going to the left. Now, is she going more to the side, or is she falling more back, or more forward? Okay? So let’s watch it again. So right away you know, hey, this left side is more… is probably involved. And listen: She’s doing this, I think, for the most part, with her eyes open most of the time. No, she is closing them. But take a look here. She’s here, and then she closes her eyes, but she opens them as soon as she starts falling. She’s very unstable. So, she’s going to the left, we see that. But she’s almost falling left and back. Do you guys see that? Okay. So if she’s going left and back, you would have a tendency to think, “What’s going on with that posterior vestibular canal?” more than if she’s, let’s say, going forward and falling, or just to the side and falling.

So those are the things that you want to kind of look in your diff-di. So when you’re looking at the sway, right, anterior canal, lateral canal, posterior canal, of these.

[20.02]

So, sometimes when someone is just standing there, you want to kind of see which way they have sway. Now they tend to sway in an oblique a lot of times, but sometimes they’re very clear on one side versus the other. So then this would tell you clinically you’d want to do different things. So now, you guys, you could put her, like, in that same position, and if you wanted to then see if her vestibular canal, her posterior canal was involved – right? – and which side: left or right? Left. You could put her in a Romberg’s, and then position her head, and her left vestibular canal, and see if she gets totally worse, versus the horizontal canal – left horizontal canal – or left anterior canal. So when you see someone with Romberg’s, if you want to see if they have any type of vestibular canal component to it, you can then put them in that position, and put them in each canal, and that will give you a clue and some understanding of that specific canal’s influence on the vestibular system, right? So it helps you go a little bit further and look at these things a little bit deeper.

Now, if you see none of the canals really make much of a difference, then you probably are going to think it’s just cerebellar integration, because they all integrate in the cerebellum as part of it. Now, you could have a cerebellar dysfunction, but one canal is really more involved, so when you engage in therapy, you may involve exercises for the posterior, left posterior canal versus left anterior canal, or versus left horizontal. So one of the things we always do – and we did this in the workshop last night – is, we put people in different head positions for each canal, and see how they do, right? And sometimes you can also have somebody anterior translate their head, and posterior translate their head, and see if getting some of the otoliths make any difference with their stability and their balance. Now, sometimes it’s purely central; it’s, like, cerebellar dysfunction, but you can find out which vestibular system can also help. So if she’s totally unstable – right? – and let’s say you put her into a… you kind of have her lean her head back a little bit, and she gets really stable, then you might do otolithic stimulation, right? Or if she’s translating back, you might put her, like, say, in a swivel chair and then push her back, or have her push herself back a few times, and if she stands up, she gets more stable, then you know you can do posterior translation utricle activity. Right? Or, if you put her in the anterior canal, and all of a sudden she’s not as bad and then gets more stable, then you would give her anterior canal exercises as a way to rehab her balance issues.

So, these are just the concepts you just want to make sure you’re understanding as we go through it. Okay. Dr. Brock’s going to go into a lot more specific examples, but I just want to make sure you get the clinical thought process going, because that’s all that really matters for us, right? You can… Here’s the thing. All


the information on the vestibular system is already out there, everywhere. The problem is, you have to know how to think through it, and how to apply it. Okay? So, most people are academically astute when it comes to vestibular system, that are into it, but clinically they’re not. That’s where you really want to focus stuff, is on the clinical information.

Alright. Now, watch her. She’s going to do one of the therapies they do in vestibular rehab is, they have people do figure eight motion, as they walk. Okay? Now, watch her walk, and just get an idea of what’s going on with her.

Walk in a figure eight pattern, three to five repetitions, while attempting to keep your head level.

First question: How’s her stability? She’s on high heels. That’s also another thing. She’s got some pretty good integrity there. Did you guys notice anything else? Did you guys notice her arm swing? She has reduced arm swing. Right? Watch her one more time just for a second. And instead of just focusing on the balance… because for the most part, if you see her, as she’s going around she’s not, like, getting unstable, going to the left. The reason you so a figure eight is because now you’re activating the right side, and then as you turn, now you’re activating the left side, and you’re trying to see if there’s instability as they activate one side or the other, and it also helps rehab people that are trying to integrate. But with her, you see something very characteristic with her is, she’s lost her arm swing. It’s pretty significant. So, think about what… These are questions for you: Which arm is it, and that thing correlates to which brain? What other findings would you expect to see?


Her arm swing isn’t going that well, but you see how that right side just doesn’t move at all? And you have to understand: It’s not that she has basal ganglionic disorder. When you’re trying to stay tight, to go around something, you keep your arms in as a tendency, so you’re not going to necessarily see as much arm swing, but you can see that that right arm – right? – that right arm wasn’t working as well as the other side. So…


Okay. So you see less activity of that right arm? Which part… which brain would be involved? So arm swing is motor activity, right? And it’s integrated motor activity, if you guys remember, right? From all [?]. So you’re looking at the contralateral side. The left side. So if she has… So what would you expect to happen with her DTRs on her right side, if her left motor area’s involved? Would you be surprised to find out she has difficulty finding words? And when she gets tired she may have a hard time pronouncing words and things? Those are all related to left-sided things. This is why, if you know your compilation charts that we’ve put together for you – if you know those really well – the minute you see one exam finding, you know what to expect and to look for, much more carefully with the other ones. And those are important to you, because once you find them, then you can monitor the patient’s progress with it. Right? Because you can just go, “Listen, hey, you’re whole left… you know, looks like your left brain’s not working. How is your word recall? How’s your right-left discrimination?” “Oh, they’re terrible.” “Okay, well, we’re going to monitor you and see how those things change with your therapy.” Right? That becomes useful. Okay.


Now, here’s a different thing I want you to look at. First of all, when you see her, do you see some change in her head position? Is she rotating? Or is she tilting? Okay. So if someone is tilting, that means they have some type of weakness impairment in a torsional muscle. Okay? Superior muscles intort, right? And inferior muscles extort. Okay? Superior muscles that intort involve the ipsilateral cerebellum; external rotators involve the contralateral cerebellum. This is general rules. There’s lots of… once you know these rules, it makes everything easier.

Now, when you look at her eye, her eyes look level. Left… Let’s look at the left eye first. Does her eye look central and level? Or does it look misaligned? The left eye. Maybe a little bit in. It’s hard to say. But what about the right eye? So again, this is going to be sometimes hard to interpret. There’s going to be differ-ences in opinion from one to the other. But this eye is involved. There’s one side is one eye. From her head position, what is she trying to do? She’s tilting her head which way? Left. Okay. So when you look at head tilts, you’ve got to try to see: You turn your head in an area to compensate where your eye can’t go. So if you look at her right eye, her eye can’t depress, right? Her eye can’t depress, so what do you have to do? You have to turn your eye out so you don’t see double vision. You have to take the pressure off of it. Okay?

So, does she have a depressure on the right? Does she have an elevator issue on the right… on the left side? So right away, you just know that there’s some muscles. Now, you have to go through your eye muscle test, and gaze, and so forth. Most of these, usually, when you see it like this, my first impression would be: this is a right superior oblique weakness, a little out to the side, give a head tilt this way, because she can’t depress, and she can’t… she’s intorting. She’s attempting to intort, because she’s tilting her head this way. So when you see someone who’s head tilts up and they’re trying to intort like that, you know that it’s probably a superior oblique muscle. But it could easily be an inferior muscle on the opposite side. But it’s the most common one.

Now, we don’t know. I want you to just think about this. So whenever you guys look at head position, that’s really important, because the vestibulospinal system is really critical in coordinating ocular muscle integrity. So when people have vestibular issues, and they have lack of input to a certain canal system, or eye muscle system, they can actually compensate with head rotation one way or the other, which then leaves them with what? Chronic muscle tightness. If you had to constantly tilt your head to the left all the time, you’d end up with, “Hey, my neck’s always tight on the left.” Okay? So a lot of chronic muscle tightnesses may be due to compensation for improper vestibular integrity. So you can actually correct a lot of chronic neck tightness issues and muscle issues by looking at their eyes and the vestibular system, and figuring out what’s involved. So as we get into the vestibular system integrations, you guys will see that the vestibular nuclei fire down to the vestibulospinal tract, which keeps the intrinsic tone of the neck and spinal muscles. So whenever you see vestibular imbalances, you’re prone to see chronic tightness issues and compensations from people that have to keep their muscles in one area all the time. Or to compensate. Okay.

[30.03]

Now, when you see her, here’s the thing. Here’s what she’s going to do. She’s going to do an exercise. She’s going to first saccade to one eye, and then turn her head towards it. So when she saccades to the right eye, she’s activating her left frontal eye field, and then she turns her head, she’s activating her right canal system, right? And then she saccades to the opposite side, you get the frontal eye field on the right to go to the left, and then she turns her head to it, which is vestibulocerebellum on the left. So she’s doing it


on both sides, as a balance, as an integrity, just to keep her… improve her vestibular integration. So it’s a common vestibular integration therapy.

Now, you can eventually, as we get into more rehab, you can do it just to one side if you wanted to, for specificity, but watch her do it. Now, when you guys watch her do it, here’s what you’re going to look for. You’re going to look at her eyes. Is she as fast going from one side to the other? Okay? Does her speed change as she… she’s going to do it several times. Does her speed get worse? Or faster as she does it? Or is it consistent all the way through? So just look at her saccade speed. That’s letting you know what’s going on with the frontal eye fields. And then as she targets her finger, see if she targets it exactly spot-on, or if she has a hypometric – means she thinks it’s here and then moves up – or hypermetric where she overshoots and comes back. So that’s what you’re going to look at, okay? So you look first what you see, and then you see what happens to it as she repeats it.

Arns in front of you, and hold up your fingers at eye level, about twelve inches apart. Keep your head still and quickly move your eyes to look at the target on the right. Then slightly turn your head to line up with the target on the right. While your head is still turned to the right, have your eyes quickly jump to the target on the left. Then turn your head to line up with the target on the left. Repeat this sequence of eyes jumping quickly to find the target first, followed by head movement to line up with the target. Eyes look right, head turns right. Eyes look left, head turns left. Eyes look right, head turns right. Eyes look left, head turns left. Perform this activity for one minute, three times a day.

Okay. So we’ll go over that. Okay. So let’s go over the concepts. It doesn’t really matter if you know some of these specific brain exercises, but you’ve got to understand the concepts, okay? So first of all, when you see her do it, when she first does it, are her saccades equal? Okay, so here’s what you’re going to first… So, let me kind of show you what we’re going to see with her, okay? And then I’ll narrate it as we go through it one more time. What you see is, first of all, she’s learning it the first reps, so she’s not really sure what to do. But then when she gets the hang of it, she’s getting… you can actually see the test. The first rep is just her learning it, what she’s supposed to do. Now, what you’ll see with her is, as she looks to her target, she has hypometric movements. Her saccade gets there, and then catches up. And you guys can watch this on the video over and over again until you see it, because you want to start to, you know, have that clinical eye to see these things. And then she’ll go here, and then she’ll have movement like that. And then as she does it, they start to become normal. And their speed is a little bit slower, and then she does it, she becomes faster. Okay? And then also notice, the first time she starts to do the first eye movement, you see her left eye muscles – eyelid muscles – twitch.

Arns in front of you, and hold up your fingers at eye level, about twelve inches apart. Keep your head still and quickly move your eyes to look at the target on the right. Then slightly turn your head…

See the eye twitching?

…to line up with the target on the right. While your head is still turned to the right, have your eyes quickly jump to the target on the left. Then turn your head to line up with the target on the left. Repeat this sequence of eyes jumping quickly to find the target first, followed by head movement to line up with the target. Eyes look right, head turns right. Eyes look left, head turns left.


See the jump?

Eyes look right…

See the jump?

…head turns right. Eyes look left, head turns left.

And now, she’s much more efficient as she keeps doing it.

Perform this activity for one minute, three times a day.

Okay. So here’s the first question: Do you think… Well, let me put it this way. If she kept getting worse each time, she kept getting slower and she became more hypermetric, so instead of doing this, she started to do… versus… right? And then eventually she smooths out with her targeting. So if her targeting got worse, and her speed… if her targeting got worse as you kept doing it, which is involved mostly with the cerebellum – the flocculonodular cerebellum, right? – if that got worse each time you do it, what would you think about doing rehab aggressively? You wouldn’t. I mean, you would really… Well, you could, but you’d have to be very, very careful, right? The amount of reps you do, and just to see how she functions would be a key thing.

Now, with her, she’s getting better and better and better doing it. So is it compensation? Or is it not compensation, right? So you guys, I think when people learn functional neurology they go through this process. First they’re like, “Oh my God, how do you know where it is?” And the big deal is just to find and localize the region. Right? And localizing the region is not that hard as you know the function and anatomy, right? Once you localize the region, this is where most people fall apart. They don’t know, when they do rehab, how much or how often, and this is where a lot of patients crash. So when you look at the quality of people practicing functional neurology, the bad ones just kind of go, “Oh, it’s left cerebellum. You do this and you do that,” and just give them all these things, and they go, “Oh, just do as many as you can,” or “Just do a few,” and they make up some random number, don’t know what’s going on, and the patient will crash. It’s going to fatigue them. It’s going to be a problem… they’re going to have problems with it. Or, they jump into therapy when they shouldn’t jump into therapy.

So one of the flow charts that we made was this one. This is, like, a key flow chart. All the way from the first module. So just to go through the key concepts is, the very first thing that we want you to use in this model, is have the patient fill out something like the brain region localization form. And what would that do for you right away? It would tell you what regions of the brain are most likely involved. You could do a history, and ask every single one of those questions. It would take you a long time. It just makes you more efficient. Hand it to them, they fill it out, you immediately have taken – I don’t know – twenty minutes off your history, at least, if not more, just from having all that. And plus, you can see it all compiled in one area, so it really saves time.

So, one of the things that we do in a workup is, before we actually do an exam is, we want to have people fill that form out and know exactly where things are. We made a vestibular localization for you for this time too, too also help you with that to some degree, okay? So you know kind of which part of the vestibular


system is involved, and so forth. But let’s just focus on this concept. So, once you know the region, why is that important to you? Because when you do an exam test, when you do some kind of examination finding, like a eye saccade, or a Romberg’s, you want to see if it’s normal or abnormal. Well, if you’ve localized a bunch of symptoms to that one region, and it’s normal, you may not see it until you do some repeat testing.

So here’s an example. “Hey, I want you…” You think they have a vestibulocerebellum issue with Romberg’s. “Hey, I want you to do this. Close your eyes. Oh, you’re good.” Versus, “You have all these spinocerebellar symptoms. I really want you to stand here, and I really want you to close your eyes, and now I want you to close them for a while,” and then you see things come out. Or you put them in a position where it’s more challenging, and then you can see things come out, okay? So it helps you push areas that you need to investigate further, and see what kinds of things you need to do, okay?

Now, the other thing is, you just might see the abnormal exam finding. When you see the abnormal exam finding, you want to do… Do they get… Did they completely… Now, what if she was doing these eye sac-cades, and as she was doing the tracking of the thumb, she tells you she has a new symptom. She goes, “Now I have dizziness.” So she’s doing this, and she’s, “Oh my God, it’s making me dizzy.” How stable is she? She’s not, okay? So this is new symptoms develop with repeat testing, very unstable. Okay? What if exam findings get worse with repeat testing? Did you see her exam findings get worse with repeat testing? No. But if she did, then you’d be really worried about the integrity, the endurance of how you would do things. And what did you see with her? Her exam findings got better. So you saw this pathway here, where exam findings improve. So you could rehab her without really major metabolic concerns. Like, this is a patient, if that was my patient with that, I would be, “Hey, we’re going to do a ton of rehab with you, because you have pretty good integrity.

As you do it, you get better and better. You adapt, everything’s cool. So I might not even do any nutritional interventions in my practice. And a lot of times, especially when I see patients that have done a lot of nutritional interventions, and they come in and they’re sill having symptoms, I’ll say, “I just want you to do some neuro stuff. So I want them to understand the impact of that in there. Because she may come in with anxiety… Like, here’s an example. Someone has vertigo, they come in with anxiety, and they’re taking things like GABA, support pathways, and valerian root, and maybe they’re even taking Xanax or some other drugs, and you know with that vestibular disorder can fire to autonomic centers and promote the anxiety.

[40.00]

So, you go, “Hey, I don’t want to add any new things to your protocol, or supplements,” or, “I don’t really care if you take them, I just want you to do some vestibular stabilizing exercises. I want you to do this for the next, like, two weeks.” She goes for two weeks, you go, “How’s your anxiety?” “Well, it’s gone.” “Great. Now you understand that your anxiety was neurogenic.” Right? So it helps to differentiate these types of things. Okay.

Now, take a look at this individual. He’s got nystagmus. So when you look at nystagmus, you want to try to see which side is the slow phase, which side is the fast phase, okay? So if this vestibular canal goes down, my left side goes down, my right side is now stronger than my left. And what does the vestibular system to? It pushes the eyes over. So when you turn your head, the eyes go to the opposite side, right? So if this eye gets pushed over slowly, the frontal cortex, the frontal eye field… See the eye’s off center? So what


do they do? They push it back. But they push it back faster, okay? So if this left side’s down, then this right vestibular system, through a vestibular optic reflex, pushes the eyes across, and then the frontal eye fields catch that thing off center, and they push it back and they push it back in the fast phase. So, when you look at this, you’re going to see a fast phase toward the healthy side. Okay? Or not. I mean, that was just an example. I don’t remember what this one’s… this person’s pattern was. Oops.

[?]

Now he’s looking left to right, because you can bring out this nystagmus with eye positions.

[?]

And see when he looks to the right, you can see that fast beat more. Goes to the left. It’s not as active. And then as he looks to the right… You see that? Okay. So that’s something Dr. Brock will go to. So you can grade different nystagmuses, whether they have nystagmus just looking straight ahead, or it really comes out when they move their eyes to one side or the other. So usually, when, with Alexander’s law, if you look in the direction of the fast phase, you’d see the nystagmus more, okay? So this was an individual who had an acute attack of Meniere’s, and he had a flare-up from one canal more than the other, and he started to have all these symptoms. Now, if you just see the nystagmus, you wouldn’t know that. All you would just know is… All the nystagmus will tell you is that one side is better than the other side is better [?]. Where’s the fast beat on this one? It’s to the right, right? So his left vestibular system is not working as well – right? – as a general concept. So the right is either overactive, or the left is down. You have to kind of interpret the case.

Now, if he had a recent infection, and you saw this, you’re probably thinking he has some type of vestibular neuritis. If he has, like, hearing loss and pressure in his ear, and fullness, you’d start to think that he has Meniere’s. So you have to kind of correlate your symptoms with their history, so you have a better idea of what’s odd. So you can’t necessarily completely diagnose what the cause of the vestibular disorder is just by their eye position. So you have to look at history, and you have to look at eye function. But then, knowing where the fast or slower phase is can tell you which side is involved, okay?

Now, take a look here.

Alright now?

Okay. Is this a vestibular problem? Well, this is a drop attack. Okay? Now, various things can cause drop attacks. Can he have a tonic seizure? Yes. It’s possible. Could he have a Meniere’s reaction and have immediate disruption of the perilymph and endolymph membrane and a sudden interacting and fire that vestibular system and then have a drop attack? Yes. That’s possible too. So this is basically a drop attack. But in a kid, usually this is a seizure response. And the parents have put this kid on a… with a helmet, so he can protect his head, because he just falls all over the place, right?

Alright now?


Okay? Now, where they fall, and what systems are active, you can, you know, these are cortical base for seizures. So you can then figure out which area that you want to activate more versus another. And then you look at your other exam findings and see if you can make a difference there.

Now, look at the DTR reflexes here. How’s that, compared to this? So, it’s hyperreflexia on the right side. So which motor cortex? Left. Okay? What part of the strip is involved? Parasagittal? Superior part of the motor strip, or the inferior part? Parasagittal. Next question: What’s the blood supply? We’re going to go over blood supply. Because we’re going to go over blood supply after the break, and we’re going to teach you… I’m going to teach you all the vasculature, so you guys have that as you go on, because it’s kind of like, you’ve learned all those different regions of the brain, and the basic functions, and without the vasculature, you’re kind of missing a big piece of it. So we’ll go over the vasculature.

Now, if her arm was involved, it would be different. If her face was in… If she had facial tone issues or upper motor neuron signs, and spasticity on one side, it would be different. But right away you know, this exam finding right here is a DTR. You know it’s probably motor strip impacting corticospinal inhibition of the anterior horn, that is not working so well. So at least you have that component, right?

Now, it’s on the right side, so then you have left. Now, remember with brain, left brain, you’re thinking that is more dominant and involved – actually the cortex – with language, right brain with visuospatial processing. So people that have impacts to their right brain usually get hemineglects, and cant really tell their where they are in the world as much. And when you look at the vestibular cortex, the parieto-insular vestibular cortex, it has its effect on the right; it’s on the right side. So when people get right-sided injuries, or right-sided prongs, they have more of a hemineglect in visuospatial orientation. When you’ve got left issues, they have more of a language problem. Okay? So sometimes seeing where their cortical signs are, you can get an idea of what’s involved with them.

Now, here is… You’re going to see someone that has nystagmus. So the question is, when you look at nystagmus, do you… where do you see the slow phase; where do you see the fast phase? So, you define the nystagmus by their fast phase. So if it goes faster to the right, it would be right-beat nystagmus. Goes faster to the left, it’d be left-beat nystagmus. It goes faster up, it’s up-beat If it goes faster down, it’s down-beat. Okay?

Okay. You guys all see that? So first question: Was it… Did you see a torsional component to it? Yes. So that the eyes also had a torsional component to it. And was it going faster up or down? So it’s a torsional with an up-beat, right? This is your classical BPPV. As the crystal gets stuck in the posterior canal, the eyes of the posterior canal move the eyes down and out, slow, with a rotational component, and then they go up. Okay? And then what you see is, this is a person that was put in a position for their canal, they started going to their upbeat nystagmus torsional component, and then as they stayed there, their crystal in the canal – right? – otoconia, got stable, so it wasn’t changing pressure in the canal any more, and then the nystagmus stopped. Okay? Watch one more time.

So I put her in position, that otoconia in the canal is causing the rotation, after a while the crystal stops moving because the head position is maintained, and you see it stop. Okay?


What if you put someone in a head position posterior and extension, and you didn’t see that characteristic nystagmus? You saw it go all over the place? Would you think it’s a specific canal? No, you guys. That’s where you’re thinking, “Hey, this is vertebrobasilar insufficiency. It might also be stopping blood flow to the cerebellum, and all of a sudden I’m getting these eye movements all over the place, right? So, knowing the direction of eye movements with nystagmus is really important, right?

[49.50]

So, one of the most common things, like, one of the things you guys just have to leave this weekend with is things, you know concepts like ototoxicity, what to do for them nutritionally, dietarily. You guys have to know BPPV – benign positional proximal vertigo. So you’ve got to make sure you guys know those eye movements, because those are things that are so common. Some of the other things that we’ll get into are not as common, but we still need to know them. But these you just need to make sure you master. Okay, so those eye movements.

Now, watch this person walk. Try to figure out what part of the brain is involved. Or the nervous system. It’s a normal gait.

Okay, you can turn around.

Is she stable? No. Could this be cerebellum? Could it be vestibular? Could it be parietal? Could it be posterior columns? Could it be large-diameter fiber neuropathy? You guys, they’re all potentially possible, just from that gait – right? – to some degree, because you’re seeing instability, you’re seeing cautious steps, not knowing where the environment is.

So at the end of the day, you’re going… Your brain has to know where you are in space. So our vestibular canal is giving information to where you are in space, right? As your head position moves, your brain’s recognizing you’re shifting to the left, or walking forward, or walking back, right? Your… All the vestibular stuff then gets integrated into the – we’ll go over to this – but the parieto-insular vestibular cortex, in the parietal lobe. All your somatic information gets associated… gets integrated in the parietal lobe, but that somatosensory information goes through large-diameter fibers, then go up the medial meniscus, that then end up in the parietal lobe, right? So those are all the things. And then you have your… you also have your conscious and unconscious proprioceptive pathways, where you have pathways that go up to the ventricle posterior lateral nucleus, and you have integration in the parietal lobe. So whenever you see instability like this, you have to differentiate which ones they are. Right? So… And you guys, when you lose one, you start to degenerate in another. If someone has large-diameter fiber loss, what are they losing input to? To their parietal cortex. And as they lose integration there, you get some degenerative changes there. As they lose their instability and start moving, what becomes more efficient over time? Their vestibular system.

So, whenever you see one, you have to look at the integration of the other. If it’s been chronic for a long time, you’re going to see compensation, degenerative changes, inefficiency in the other spots too. So you always want to make sure you go through the entire checklist of things that are involved. Check the posterior columns, vibration sense, check aspects of parietal lobe function, check the vestibular canals, and check the cerebellum. Those are all what’s involved with making sure that you’re in space.


The fact she’s walking like this is letting you know that one of those systems is off, okay? Now, she has diabetes. Okay? She has neuropathy; diabetic neuropathies. So she can’t feel the ground. So watch again. So she can’t feel the ground, so she’s unstable.

Okay, you can turn around.

She’s got to hold on. She doesn’t get that feedback going on. She’s totally counting on her vestibular system. Now, what if… Would you evaluate her vestibular system knowing she has diabetic neuropathy? Yes, because what would happen if you make… She’s… Her whole func… She’s depending completely on her vestibular system. So if you make her vestibular system even more efficient, how will she function and get around? Better. You guys understand? So when you lose one, if you have better function in the other, you can compensate for it, and you can have better function. So obviously you would want to control the diabetes, and look at the inflammatory reactions happening at the peripheral nerve – one clinical model – but now you go, “Hey, what’s going on with her parietal lobe? Has it degenerated from lack of activity? What’s going on with the vestibular system? If you can get her vestibular system and parietal lobe functioning better, she’s probably going to get around in the world easier, and function better, because her compensation systems are more fine-tuned.

So, let’s say you go and you do some testing, and let’s say when she does finger-to-nose, you see a little bit of tremor, but when you put her at one canal position, it goes away. Or it’s improved. Then you might do canal therapy in that one area. And we’ll get into therapy, but I just want you to understand the concepts. Okay.

Watch this guy walk.

[jumbled conversation] The next part is to do the same thing. This time you’re walking heel-to-toe. And if you need support… [jumbled conversation]

Okay. We’ll over it and break it down piece by piece. First thing I want you to… First thing I want to kind of discuss is, how’s his posture? Is he erect? Does he have good posture, or is he forward, or… Okay. Now he’s forward, right? So he’s going forward. And what do you think his tone is to his… So there’s several possibilities. He could be bent forward because there’s something wrong in his spine, right? So maybe you have a hyperkyphosis. That’s a possibility, but usually you see that in the upper thoracic area more than other. It’s not really that characteristic pattern. But it’s something that can cause someone to bend… to be positioned forward like that. What’s another possibility? Well, he could have Parkinsonian pattern – not that he does – but if you have a Parkinsonian pattern, they lose their center of pressure and where they are in space, and they use their postural reflexes, so they feel like they’re falling back, so they reflexively move forward. But with them, you would also see what? The hands turn in, and lack of arm swing. You kind of see them walking like this. It’s not that, but that’s something that can cause a person to have that forward sway. Okay?

Now, the cerebellum fires to the spinocerebellar tract, and you have vestibular input that fires into ves-tibular nuclei, and you have the vestibular… mediolateral vestibular spinal tracts, with the spinocerebellar pathways that then activate the intrinsic spinal muscles. So one of the things that you see, when people start to lose their vestibular tone, or the vestibulocerebellar tone, whichever system’s involved, is you start to see that they lose their intrinsic spinal tones, so they tend to have lost their posture, and they’re forward


like this. Okay? So you guys see kids, hypotonia forward like that, you just know they’ve lost their tone and so forth. So with him, you know first of all, the vestibular tone is off, okay?

Now, let’s watch him… Or unless, you know, there’s something going on with his spine. Watch him walk. You see change in arm swing. How’s this arm compared to this? So he’s got a reduced right arm swing. You guys all see that? Okay. So is this the vestibular system, or is this the cortex? The cortex. And his arm swing is less on the right, it would be what? Left cortex. That’s involved to some degree. Okay? Now watch the rest. He’s moving around.

Does he sway to one side? Do you see his body tilting to one side? See him going to the right?

[jumbled conversation] The next part is to do the same thing. This time you’re walking heel-to-toe.

So what does he do when he stands? Wide stance. He’s not standing like this; he’s like… Okay.

And if you need support… [jumbled conversation]

This is not a proper test for ataxia. This person whose testing him doesn’t even care. I mean, the guy’s looking down and he’s speeding through it. Okay? What you want to do with this is you want to have a person look straight ahead, and then go a little bit slower so they actually test their muscles. When people lose their balance, they work with their fall, and it looks like they’re actually better than they are. So if you slowed him down and put his head up, you probably would see him have titubations. But the fact he’s looking down, and he’s still unstable, lets you know his what? Vestibulocerebellar could be involved. Could it be his peripheral nerve? Could he have a proprioceptive issue coming in from his feet? I mean, it’s possible, right? Those are all things that you have to investigate.

Which way is he falling? Sometimes he’s going to the left, now going to the right.

[jumbled conversation]

So he’s completely unstable. There’s involvement probably in both sides. Now, is he getting better or worse as you do therapy? Okay. So what should you do? You should do, like, twenty minutes of core exercises every day, put him on a platform plate, do all these things… Let’s really give it to him. No. That’s how you would make this person totally fall apart. Okay? So again, you’re seeing it right in front of you. You’re seeing as he does tests, he’s breaking down. So remember that flow chart, with repeat testing? Repeat testing could just mean he’s walking more and more steps. And as he keeps walking, he starts to actually, instead of just walking normally, the first time he walks he’s walking down the hallway with a little bit of sway. As he continues to walk, he’s actually hitting the wall. So that means his endurance is involved.

[59.59]

Now, here’s the thing: Let’s do a quick initial survey. What… Do you think he might have any type of metabolic diseases? Well, I mean, just… you could… Just the fact he’s overweight, you have to suspect, does he have metabolic syndrome? Does he have insulin resistance? Does he have those issues? That could be some things to look at. But we don’t really see much more of that involved with there.


Okay, now take a look here. What’s your initial survey? Left ptosis, and how about facial tone? Maybe less tone here. You’ve got to see how she speaks, when she functions, her motor activity. And is she… Do you see a head tilt? See a head tilt, a head tilt to the right, okay?

…going to touch this side of your face, then touch it over here. Can you feel that? “Yes.” Is one side different from the other? “Probably, yeah. The left of my face, it bothers me. It’s not a comfortable feeling.” It’s different. “Yes.” How about here versus here?

Okay, does she have any deficit with her language? Can she speak fine? Does she understand questions? Yes. So you know her language centers, her left cortex is intact. And you’re not surprised to see that, because you’re seeing left-sided symptoms, so it’s mostly involving her right. She’s be concerned more for, like, a hemineglect, right? Now, you can see that she has that facial dropping there. You guys see that lower facial paresis that’s there? See that ptosis that’s there, right? And then she has some sensory loss. Or…

“The left side is not…”

…abnormal perception.

…if the skin were numb, then it’s barely feeling.” Barely feeling. So you feel better on this side? This side would be normal? “Exactly. Normal, I feel very normal on the right side.” And this, here, here, and here? “It’s different. My skin feels like sunburnt.”

So she has abnormal sensory perception. Her parietal lobe isn’t integrating. Now, what part of the brain controls facial muscle tone? On the left? The right motor area, and the parasagittal area, and superior or inferior? Inferior, right? What’s right next to it? The somatosensory cortex, where you have parietal integration right? You have motor strip, and then you have the sensory strip. What’s the vasculature there? Medial cerebral artery. Now, it could be medial cerebral artery, but we don’t know. We haven’t done exam findings. It could be the medial cerebral artery superior division, it could be part of the stem, she could have an internal capsule issue. But we’ll go over all that a little bit later. But I just want you to understand that, because the next thing that you have to really understand in this module, which we’ll get into after the break, is vasculature. You want to make sure you know your regions and you know your vasculature, okay?

Now, let’s take a look at this thing right here. What’s that? Clonus. On the left foot, what part of the brain? Right. So the corticospinal. Somewhere, anywhere from the motor strip all the way down to the corticospinal tract, is impaired. Okay? Some type of injury, some type of dysfunction is there.

So as you look at those… So here’s the thing: Each area of the brain has a characteristic pattern. You guys saw clonus, you guys saw hyperreflexia, you saw spasticity. So you know it was the motor strip. You saw sensory integration loss, so you know it was the parietal lobe. Right? You saw people that had ataxic gait, so you know hey, it’s got to be the peripheral nerve feedback. It could be the parietal lobe, it could be the cerebellum, it could be vestibular system. Those are things that you know. You see hyperkinetic activity, you know it’s the basal ganglia indirect pathway. If you see slowness, it’s hypokinetic activity, right? Frontal, hypokinetic projection to the basal ganglia indirect pathway. So each part of the brain has a characteristic pattern. You can’t learn the characteristic… So, as soon as you learn your characteristic patterns, with their


function, this whole game gets easier. What most people do is, they just try to associate a finding with a treatment. Do not do that. That is a failing model.

Now, when we talk about the vestibular system, it’s the same thing. Each part of this vestibular system has a characteristic pattern. A right posterior canal versus a left anterior canal versus a horizontal canal, versus a saccule, versus a utricle, are different. Inflammation to the vestibular nerve is going to be different presentation than a fistula. Right? Or a Meniere’s rupture of the thin membrane of the… They all have a characteristic pattern, just like the brain. So just like you learned all the concepts of the brain, you want to make sure… This weekend we’re going to teach you all the characteristic patterns of the vestibular system, the peripheral vestibular system, so you know how they are, how they clinically present, and what their exam findings are, and whether it’s related to nystagmus, or their sway, or their eye movement, or the positional area. You can then identify the area. Once you identify the region, then you go in and do therapy, right? So that’s the goal, is to make sure you have that clinical eye for each one of those things.

Okay. Dr. Brock is going to go into some cases with you, and then integrate some of this information more for you. Okay.

dr. brock.

Mic on. Is this mic on? Yep. Can you hear? Alright.

So, good morning, and jolly Saturday. Review of concepts here, huh? Peripheral vestibular system. I think it’s always good to continue to bring previous material and sort of take it in to this class, so that you can continue to integrate the big picture. I think without doing that, it’s really easy to… everybody to kind of get involved in their life, you know, you’re taking care of family, you’re doing your practice, or you’re a student, and you don’t get to study quite as much as you want. And so I think that this is… You know, Dr. Kharrazian and I kind of decided that we wanted to make sure that we give you the opportunity to see a little bit of information from previous classes. So, you’re going to indefinitely have questions this weekend. If you do, send your questions to [email protected], just like we always do. And please remember to sign the sign-in sheets. I was told to tell you all that. So anyway. Let’s get going.

Well, you remember this chart right here, and we have additions to this chart that I’m going to start putting up. How many of you saw, at least on the member section, all the videos that I made on speech that broke them down? No? Yes? Raise your hand high. I just want to see, because… Okay. We’re working on getting those put onto the website as well. But I took all ten patterns and broke them down each one individually, so that you would be able to understand clearly what Broca’s is, clearly what Wernicke’s is, and all the ones that are in between. I think that’s important to kind of note, that we’re adding ancillary videos as we kind of go, and when we get feedback of what people need. Because we understand that there’ll be just some topics that people will be like, “You know what? I don’t really get it.” Or, “You know what? I do get this. Let’s just move on.” So even this weekend, tomorrow, like I said earlier, we’ll be doing… I’m going to show all the repositioning maneuvers, and all the provocative maneuvers for the peripheral vestibular system, up on stage, so that we don’t have to go back and make some of these ancillary videos. It’ll just be a part of it.

But we’ve kind of talked a little bit about the lobes of the brain, and hopefully you’re kind of now starting to see some of the integration of the forms: the brain intake forms. And you’re kind of learning what some of the left-brain functions are, some of the right-brain functions are, and as your patients come in and you


talk to them, you can say, “Wow, this person looks like maybe they have some left-brain problems,” or some right brain problems, or some global problems. One of the things we talked about in the workshop last night is, there really is no linear model, where just one hemisphere doesn’t work, and then one does. That does occur, in some people are extremely dominant in one hemisphere, or extremely deficit in another, but we’re also finding that you may have a little bit of damage in one hemisphere and a little bit of damage in another, or just global degeneration that happens in a pattern.

Like what we talked about last module, with neurodegenerative diseases. Is it hippocampus and frontal lobe, and a little bit of these spatial awareness area, like with Alzheimer’s? Or is it frontotemporal demise, or corticobasal demise? I’ll go through some of those here in just a little bit. But looking at these lobes of the brain, it was really interesting even last night. We saw a lot of this. Problematic, you know. We saw everything from vestibular pathology to cerebellar pathology to cortical pathology.

And then we know that the basal ganglia has this direct pathway that makes you go, and this indirect pathway that makes you stop, and when there’s an imbalance in one versus the other, we get pathology, and we kind of talked about that. We have this cerebellum, and then we have the midbrain, and the midbrain integrates a lot of the vertical eye muscles. And this is where I’m going to add a little bit of additional information when we look at some of the verticality, and the inability to look upward, or some vertical skew, or different things that have to do with that.

We might want to start looking at, is there a mesencephalic… Now, mesencephalic is synonymous with midbrain. Same thing. So the midbrain is your mesencephalon. It goes medulla, pons, mesencephalon. And I believe that Dr. Kharrazian is going to break down some of the brainstem anatomy for you, and just teach it to you in the rule of fours. So we’ll make it pretty, pretty… I say simple. The brainstem is considered no-man’s land in neurology. It’s like, nobody wants to learn it, but if you teach it the right way, it’s not really that difficult.

[1:09.59]

Over here, this little guy right here. You can see it. The vestibular system. It really is my favorite system, and I guess it’s one of my favorite systems because I understand it probably a little bit better than most of the other systems. And it’s not quite as vast as, like, the cortex. The cortex is one of those things that’s still being researched. We barely know anything about it. And ten or twenty years from now, it’ll be completely different. But the peripheral vestibular system is the peripheral vestibular system. That’s why I like it so much. It’s very linear. You will know the difference between BPPV and neuronitis, hopefully within five seconds of the patient walking in.

And I really… No matter what kind of practitioner you are – and this is the big point, I think this is one of the big draws to this class – is that if you’re a neurologist, and you don’t know these conditions, you might have to think about checking in your neurology card, right? Because this is real neurology. But if you’re in family practice, this is where most people go that have these BPPV conditions, or these benign – you know, they’re not all benign – but some of these peripheral vestibular conditions, they go to their family doctor, because they’re like, “Look man, something’s not right.” Or they go to the ER, and the ER’s like, “I don’t know what to do. Here’s some Antivert, or some meclizine. See you later. Go see your family doctor.” And they don’t end up in the neurologist’s office until everybody’s failed. That’s the truth. And here’s how


I know it’s the truth. I’ve done a hospitalist rotation before, and I walked into an area where there’s, like, eight residents, and one chief neurologist, and they couldn’t figure out what the person was, and nobody did a provocative vestibular maneuver on the patient. They sat there for hours pumping drugs into the guy, and he was going crazy, and all it took was a simple Epley maneuver, and the guy got up and basically put on his clothes and left.

Now, that’s not to say that those doctors are bad or good. It’s to say this: This material has kind of been left… The peripheral vestibular material’s been left. Even the functional neurology world, they want to skim over it, because they assume that you learned all of it in school. And really, I don’t agree with that. I didn’t learn much of this in school at all. And if I did, it didn’t stick, because I never saw a clinical case. So I want to make sure you get it, so that you don’t miss these real subtle – you know, non-subtle, very obvious – peripheral vestibular pathologies. You have… About twenty percent of your vestibular cases are going to be these. And I’m giving you a low… I’m low-balling you on that.

So, we have to determine: is it central versus peripheral? And of course, next module, we’ve got the central ones. This one we have the peripheral ones. We don’t want to really intermingle them much, because if we do, it gets even more confusing than ever, so we just want to say: let’s just stay on the periphery. And then we’ll show you the integration, and we’ll lightly integrate into it, and then we’ll come in and we’ll say, “Hey look, here’s the central ones,” and then, “Here’s the difference between the central ones and the peripheral ones,” and you’ll be able to differentiate them very easily. Hopefully.

We talked about autonomics. Now, with vestibular pathologies, there’s autonomic changes. With cerebellar pathology, there’s autonomic changes. With cortical changes, there’s autonomic changes. Listen: People that have fear responses have autonomic changes. People who are on medications have autonomic changes. People who are on recreational drugs have autonomic changes. So what I want to tell you is, autonomics are used as a way to measure whatever it is that you’ve found, if it’s getting better or worse. Because a lot of times, autonomics are a window of: is that part of the brain that you’re treating changing its integrative capacity into autonomics? Why do most areas of the body and the brain integrate into autonomics? I’ll give you the answer. The answer is, there’s really not enough blood to do everything at a high level at once. So the body has the ability to say, “You know what? This area has to perform at a greater level because of demand, like moving your arm, so let’s shunt blood there.” Or, “You have to think, or do a certain thing cortically, so let’s shunt blood there.”

One of the problems, as we get more advanced, and we show you things, is that a lot of times when a certain part of the brain has a metabolic demand, blood gets shunted to another area because of aberrancy. Then you become very efficient and that part of the brain fails.

So, autonomics are a really beautiful thing to learn how to measure. And here’s the thing: Autonomics will kill you slowly. How many of you understand what I mean? So in other words, blood pressure. If it’s too high, a lot of times you don’t just fall over dead from a stroke, but over time, your heart gets bigger, your left ventricle doesn’t work as well, there’s more total peripheral resistance, there’s strain on your kidneys, you start to destroy nephrons, and you slowly fall apart. If you have stress, and your catecholamines are up, or your cortisol is up, it starts to slowly deteriorate your brain, and your hippocampus may die off, and your short-term memory may go away. So I like autonomics to be at a state of peace. I really do. I really… And then I like to evaluate people’s lives by questioning, and saying, “Look man, what is it in your life – if there


is something in your life – that is driving up your autonomics? Are you living with people that are driving you kind of crazy? Are you in a bad situation? Are you stressed out? Are you eating bad?”

And then, you know, counsel people in saying, “Look, you have to change your life to change your stress, so that your stress doesn’t change your autonomics, so that your autonomics doesn’t promote chemicals that deteriorate your body and your brain at a faster rate. And then you have to change it and you can’t go back.” Because if you go back, what happens? You have a patient for life. They just go back to the way they were, and they come back in with the same condition, usually worse.

So, with autonomics, it’s a window to life. Okay? Motor output is one of those beautiful things where we look at gait, and we can say, “Wow, you’ve got a peripheral neuropathy,” like we saw a second ago. Or, “Man, you’ve got an ataxia,” like we saw a second ago. Or, “Wow, you have a Parkinsonian shuffle. Your motor function,” – when you get really good at looking at motor function you can say this – “It’s brain.” Or, “It’s stroke,” like we’re going to look at in a little bit. And if it’s stroke, is it in a terminal vessel? Is it in the internal capsule? Is it in the main trunk? Where is it? You can say, Is it spastic, like with a corticospinal lesion. Is it rigid, like an extrapyramidal basal ganglionic lesion? Is it floppy and hypotonic, like a cerebellar lesion? Is it weak and atrophying, and losing tone, like a lower motor neuron lesion that denervates?

Motor function is really the biggest window we have as a functional neurologist. It’s a beautiful thing. We look at it, and we go, it’s everything from language, the way we talk, right here… It’s everything from motor function, the way we posture ourselves and move our arms when we walk, and the way we move our legs, and the tone that we have, and the facial expression that we have, and the facial symmetry that we have. And then as we go on, we’ll teach you. Here is a good sensory exam. Because without good sensory input, we have bad motor output. And with bad motor output, our human capacity goes down. And when we lose performance of autonomics, and we lose performance of motor function, and then we lose control of our autonomics, our brain will start to suffer, we’ll start to deteriorate, you’ll start to turn on certain genotypes, and it will promote neurodegenerative disease, like we talked about last module. That’s the process of aging. I would just rather do it slowly and gracefully rather than rapidly, like a boulder going down a hill.

We know that when we have bad autonomics, and we have a bad brain, and we have a lot of inflammatory or traumatic responses, we have a greater chance of having pain, and we know that if you have pain, it can promote limbic responses. Now, what I mean by limbic responses – and I’ve just decided that I want to slow down and break down words for you – limbic means emotion. The problem with a lot of limbic responses, is their emotional responses, but they’re survival responses, which means they’re not always cool. They’re like, “Uhh!” They’re fear responses a lot of times. So in the limbic system, there’s a couple of areas that you need to know. There’s the amygdala, and then there’s the nucleus accumbens. And the amygdala’s out sere sort of living in the temporal lobe, really deep, and it’s raw emotions, it’s fear responses, and it really gives you awesome facial recognition capacity. Why do you think facial recognition capacity is so amygdalar? Let’s remember the person that attacked us, so that we can haul butt whenever they come around. And the amygdala ties right into the sympathetic nervous system and gives you a flight or fright response. You’re orbitofrontal system comes down and inhibits the impulsivity of the amygdala. That’s why I told you: orbitofrontal systems, when they go down, people get what? Impulsive. Their amygdalar system just goes whitwyoo. It’s do whatever it wants. It’ll blurt in, it’ll get scared, it’ll get worried, it’ll get concerned, it’ll jump in, it’ll interject, it’ll do some really bizarre things.


[1:19.56]

Meanwhile, the nucleus accumbens – which is really part of the basal ganglia, and dopamine fires into it, and then it goes to the direct pathway, and everything gets happy – becomes efficient. “Oh wow, man. Exercise. That felt good.” “Whew, that cocaine was awesome.” “Man, that heroin was so great, I want to do it again.” And that goes up to the dorsolateral prefrontal system, and your cortex ends up saying this: “Man, that’s good stuff, but we can’t do this.” So the only way we can overcome that whole process is willpower. Like, by taking a substance. Your orbitofrontal system looks at the amygdala and inhibits it. So when your frontal lobe goes down, you get scared, easily controlled by substances, needing outside substances, needing outside chemicals, can’t focus, can’t pay attention, and then we can start to divide it into right or the left.

So, as we go through this, the understanding of the cortex will get a little bit more advanced, okay? Over here in language, I’m going to show you some stuff here in a minute on what these mean again, and then over here, motor, we just talked about tone, compartment control, and coordination. So when you look at this diagram, you should say, “Wow man, this kind of represents a lot of stuff. Where do some of my patients fall on this diagram?”

Okay. We’ve already talked about this. I still love this flow chart. I love to be able to really… Let me give you a piece of advice on what you should do with this. Take this and print it and laminate it. That way you can draw on it with a sharpie. Or, just make a bunch of copies of it, so that you can draw on one for each patient. And then what I like to do is, really, you kind of get to where you can do it in your mind, but it’s really nice at the beginning of this to say, “Okay, look.” You circle this section right here, and you say, “What did I find in my neurological exam?” And you write some stuff down. And then over here, maybe you write some exam findings. And then if repeat evaluation makes endurance, you check endurance. If it doesn’t, then you just scratch it out. And then, you know, you just follow this all the way through, and you won’t believe the answers you will get when you just start thinking in a linear fashion about your patients. I think this is a nice thing to use, because it keeps you on track, and it trains you to do the same thing on each patient. “What did I see? Can I change it? Can I not change it? Does it fatigue? Does everything make them fatigue? Does it look metabolic? Does it not look metabolic? Do I need to do…” – and Dr. Kharrazian and I were talking about this last night – “Do I need to do both a functional medicine and a functional neurological model?” And if you know both, does it make you cooler? Not really. You don’t always have to apply both to each patient. But sometimes, your clinical skill will teach you when you apply one versus the other.

So, knowing this stuff, let’s look at a patient. So, right off the bat, when you look at this gentleman right here, you notice a couple of things. And I would say that one thing I would notice is the fact that he’s wearing glasses. Why does that matter? Well, maybe he doesn’t see well. Okay? I don’t know what that means. I don’t know if he has trifocals, bifocals, if he just wants to look cool. I don’t know. He’s got a little bit of a head tilt. He’s got a little bit of body rotation on the head. He’s got quite a few things. You can see right there that his eyes are not straight on the horizontal. This is nothing but an observation exercise. This is not a localize-the-level-of-the-lesion exercise. And we can see right here that his mouth is a little bit straighter. But you can see a little bit of changes in one side of the face right here, versus the other. But his nasolabial folds are pretty symmetric, and he doesn’t seem to have facial paresis. But is he masking? Let me ask you this: Does he look absent? He looks absent.


Now, you always want to be careful on this, because you can catch people in a picture in the middle of a movement, where they may look happy, surprised, angry, masked, or whatever. So any time somebody shows you a picture of somebody and they look masked, make sure they’re just not looking at you in total blank astonishment. See his head? So he’s angulating off. Little bit of change over here on the right side. His mouth is pulling over here to one direction; not pulling quite as much over here. The wrinkles are a little bit changed on this side versus this side. I’m just giving you things to observe.

Now, let me ask you this: If all of this up here is preserved, but let’s just say that this lower quadrant is not, which cranial nerve might be involved? So, 5 gives you sensations, 7 gives you movement. 7, whenever it gets damaged at the level of the facial nerve, will typically affect this whole side. But whenever you just have one lower quadrant that is changed, it is usually a corticobulbar – bulbar meaning cranial nerve – that is the brother of the corticospinal tract, which goes to the spine. It still does this, ladies and gentlemen. It still crosses over. So if we were going to do something, like, really crazy here, and draw a picture, it would cross over. If this whole side is involved, we would say, “Wow, maybe the facial nerve is swollen as it goes through its frame, and you have a Bell’s Palsy – older term for facial paresis. If that lower quadrant is involved, maybe the contralateral motor strip is starting to stroke a little bit, or be damaged, or something’s going on, and its output is not that great.

Now, these are all very subtle signs. I’m just sort of throwing some concepts out there so you start to learn how to observe a face, because we’re going to look at brainstem, and the brainstem has cranial nerves, and the cranial nerves all go to the head, except for some of the lower ones, which go down to the organs and the viscera. Is that cool? Everybody in here that is clinically going to be looking at patients, there is no such thing as a specialty that should ignore this. Right? You’re like, “I’m a nephrologist.” So? What if somebody comes in and had a cortical stroke and now they can’t move their face? Maybe their GFR is not their biggest problem at that point, alright?

So, this patient is starting to get a flat affect. Did you notice that? Flat. Now, what does a flat affect tell you? Let’s go back to that initial chart. Does it tell you their cerebellum is off? Primarily. Maybe not. But does it say anything about maybe their frontal lobe and their basal ganglia? Yeah. If the direct pathway is winding down, and their cortex is not being activated, maybe they’re flat. If their frontal lobe is being damaged, maybe they’re flat. So when I see that kind of masking, I just want to say this: “This doesn’t look like a very energized system to me. I would like to see this person come back to life. Because right now they look goners. That’s not good for what I would call his humanity.” He’s getting a reduction in spatial understanding In other words, “I don’t know where the grocery store is any more.”

Okay, now what a minute. Let’s go back to last module. He’s losing spatial awareness and how to get around, and he’s starting to get a flat affect. We haven’t asked him any questions yet to see if he can remember. But what was one of the very first things that you saw in early dementias? Some? A little sliver back here, espe-cially in, like, and Alzheimer’s dementia, where somebody, like, all of a sudden they’re – at night – they’re like, “I get confused very easily.” It’s one of the very first things. You don’t want to hear that. Like, “I’m missing words. I’m skipping words. I can’t find words. And I can’t get around at night because it’s confusing to me.” Because they can’t see the landmarks as well. Most people can drive from one place to another that’s familiar, and just see a couple of landmarks and make it. But when it’s dark, maybe those landmarks are not as visible, so they can’t navigate. So they become disoriented. Bad sign, ladies and gentlemen. The patient has no loss in fluency or reception, or perception. Okay? The verbal fluency. Alright? The patient


has short-term memory loss though. Uh-oh. So now they’re getting what? Spatial perception and, “How do I get from A to Z,” and, “Now I’ve got a flat affect,” and, “Now I’m starting to lose short-term memory.”

How many of you could start to just draw the brain out, and what is starting to deteriorate? Do you think the frontal system is more damaged than the posterior system? Yeah, he’s flat. Do you think the hippocampus is more affected than… or do you think it’s affected? Yeah, that’s where short-term memory is. So you start looking at this person, and you’re like, “Man, this could be hippocampal, frontal, neurodegenerative, flat affect, progressing, spatial awareness, but they’re not losing speech yet.”

[1:30.04]

Now, why did I say anything about speech? Did speech give you the capacity to differentiate something like a frontotemporal demise, or a corticobasal demise versus Alzheimer’s versus another neurodegenerative disease? Remember I taught you those little nuances of subtleties that taught you the difference between each of those? You want to know, right out of the gate, is there, you know, a primary fluency-in-speech issue? Well, this guy doesn’t know his own address. So let me ask you a question: Is this stage one? No. This isn’t stage one. He’s in trouble. Is he at least a stage three or four? Maybe even a five? Yeah. He didn’t know what day it is. So what do you think this is? Do you think this is just left hemisphericity? You think this is cerebellar disease? Do you think that he has other problems? Look, let me assure you of something: This is dementia. We don’t know if it’s vascular, we don’t know if it’s Alzheimer’s. It looks like it’s probably Alzheimer’s. But here’s the thing – and this is the question that I really need to ask you – if you want to really work this person up, could you do some stuff that might fire up his brain and make him look a little bit better, and then you say, “Oh, he’s going to do great, cured, see you later,” and then you send him out the door, and then everybody assumes that this person’s going to be great? But what you may not see is what happens to him four days later, when everything goes hluthluthluh, crashing down again. Why might that happen? There are other underlying factors to this patient.

Now, there was a paper posted on the forum about Alzheimer’s disease being cured in six out of ten patients because of a protocol that’s being used, and the protocol has a million variables to it, and we don’t know what combination it is. It’s very interesting. And it’s sort of like what we’re teaching you. But there is no protocol for these patients. I want you to understand something. Because this guy might have five infectious diseases. Or this person may be under tremendous stress. Or this person may have zero testosterone and no estrogen. Or this person might have the worst vascular disease you’ve ever seen. Or this person may have insulin that is just completely out of control, and therefore promoting neurodegeneration. So what we found is this: Out of ten patients with this condition, they all look different. So how do you protocol that? You give seventy things, and hope that they all work. But how do you know that some of those things in that seventy-variable protocol didn’t slow… didn’t make them worse? Because it altered their immune system and made them more inflamed? Or created more antibodies? In other words, it’s not as simple as saying, “Here’s ten patients, here’s a protocol. Do everything in it, and just hope to God it works,” and it works in six out of ten people. What about the other four? In other words, there’s a lot more to it. What I’m telling you is, these cases are individual, but you have to at least learn how to recognize it’s dementia, and what type.

So, I don’t know if you remember this chart or not. But this person had a neurological condition. I just described it. And we had to determine the complaints. And we used intake forms, we used questionnaires, and stuff like that, and then we had to determine if there’s any comorbidities, like I just said. Like, does he


have diabetes? Does he have an infectious disease? Does he have this? Does he have that? And then we have to say, “Hey, which one of these regions does it look like it is?” Well, did he have an aphasia, right here, as the primary complaint? No. Was there language problems and alien hand? No. Did I describe dysphasia, dysarthria? No. Ataxia? No. Tremor? No. So you go down this, and you’re like, “Wow, the only think it looks like is spatial and short-term memory. This looks like an Alzheimer’s hippocampus presentation.” So, can you use this form to help you with dementia localization? Please do. Please do. That’s why we gave it to you.

Now, why does it matter? Because some of these are dopaminergic and basal ganglionic based. Some of these are hippocampal, cortical, and cholinergic based. Some of these are vascular, and vascular predis-position based. The treatment matters, from a functional neurological perspective, and from a nutritional perspective, and sometimes even from a medication perspective. If you get the wrong one, it just… It drastically does not work. So for instance, if you give somebody with a Parkinsonian issue, and their direct pathway’s shut down, and you give them something to ramp up acetylcholine, what does acetylcholine do to dopamine? It dampens it in the basal ganglia. So you make them more hypokinetic. Bad idea. Okay? Just… And you can do that with nutrition too, just not to the extent. So that’s why it’s like, hey look, understanding the neuroanatomy and the functional components of this helps you do nutrition just much, much better.

So with these patients, if there’s neurodegenerative disease, we know there’s going to be fatigue and changes in function, and we know that there’s going to be reactive oxygen species within their brain, probably, and we know that there’s going to be fatigue, cells are dying, and there’s going to be cerebral volume loss over time. So let me just put it to you this way: Everywhere there’s a box, I’ve got to come up with an answer as a clinician.

Okay. So this person has a given neurological condition. Which one is it? That’s over here. And this person has some things on the form that need to be evaluated, and I need to look at it and say, “What could be the comorbidities that are causing the underlying metabolic problems that are causing the fatigue, that are causing the inflammation, that creates the cellular death damage and ultimate volume loss?” Of course some of it’s going to be genetic, but a lot of things promote that. So you go back and you answer these boxes. A lot of times here’s what you do. You take this form, you print it out, you take the first form I gave you – which is all the areas – you check off all the areas involved. Then you get your physical exam and you check it off, and you check the things off that are on your physical exam, and what you need to do, and so forth. And you come to something like this, when you think it’s neurodegenerative disease, and you start checking this off, and you’re like, “Man, I’ve got to do this metabolically,” and, “Man, this is the area, and I know that these are the areas that are problematic, and when I get this person metabolically stable and capable and doing better, I’m going to start activating the areas that are not doing well,” like the hippocampus and the frontal lobe. And when you bring them both together, what you see is, cellular stability, hopefully. You may not reverse volume loss. But you may increase the function that you have left. Is it better to catch them early or later? Early. Alright.

So, we make these little diagrams so that you can use them. Feel free to print them off, check off where the areas area at, and start using them as a road map to get through your day. It doesn’t mean that you’re going to have to use them on every single patient once you get better at it. But early on, use it, and say, “Wow, I can recognize the difference between corticobasal degeneration, frontotemporal demise, and Alzheimer’s disease.” Big deal, and I love the fact that people are learning how to do that. It’s none of those.


So, when you look at this – now, this is not the best, sorry, the best… a little bit blurry – but when you look at this, you’re like, “I don’t think this is stage one, I don’t think this is stage seven,” but you think it’s probably somewhere in here. And so they can’t recall their own address or telephone number. This person’s starting to fall into stage five.

Now, let me tell you something real quick. Stage one, stage two, many of us in this room vacillate in and out of that, again, during the day, depending on your fatigability. You get to stage three, that’s when you really need to start getting treated. Four, it becomes more difficult. Five is really, for me, the cutoff limit. Because at stage six and seven, there’s not a whole lot I can do. So again, we go back to people that publish papers, and they start talking about Alzheimer’s disease, they don’t even put the stages of damage that’s in there. What does that mean? I mean, what stage are they in? Are they all stage two? Well, that’s not near as impressive as if it’s all stage six. Then I’m going to be impressed about what’s going on. Where do most people get diagnosed? Four, maybe five. Because people do not want to go in to the doctor and say, “You know what? I’ve lost my mental faculties.” It’s embarrassing, it’s hard to do, and a lot of people don’t do it until their loved ones do what? “It’s time for you to go to the doctor.” Okay?

So, look at this hippocampus. Remember this form? We gave you this. We made you these. And so you can go back, and you can say, “Okay, look. This falls under this dementia category. I think these are the areas that are involved. If these are the areas of involvement, let me go to my forms that say, hey look, what do we know right now? Without expanding these, what do we know right now about the forms that we’ve been given? Well, I think that there is a hippocampal problem.” Is there memory loss? Check. Is it impacting their daily livings? Check. Dates, yes. Events, yes. Memory loss, yes. Visual memory, yes. They don’t know where they’re at. Forgetting where they put things. Forget about their keys; they don’t even know what day of the week it is.

[1:40.09]

We don’t know about faces. We didn’t ask them names. Because now we can start looking at, you know, left versus right, and so forth, but we evaluate their recall, all of this stuff will be messed up. Now, we can do things like remembering words, remembering, like, where to go, doing… I taught you this last time. Doing the visualization of how to get from one place to the other, and then recall memory about, like, colors of what clothes people are wearing, what their face looks like, what the address is. We can recall all those things, if they have the metabolic capacity to do so. So if this guy has seven comorbidities that’s destroying his brain, and I just pretend – I’m a functional neurologist – I pretend none of that stuff exists. All I’m going to do is just give you a bunch of dates that you’re never going to remember. And I’m going to give you a bunch of instructions that you’re never going to remember because your brain is like cranking an old car that has a dead battery.

But then when you go back, and you metabolically enhance that person, and you give them some mitochondrial support, or you reduce some of the intracellular damage, or you do something to clean out cellular debris, Or you do something to give that cell endurance, and make the environment not so chaotic metabolically. Then you go back and you start to subtly stimulate this person’s brain, they start to respond to you a little bit, and some of it sticks. Make sense?


So when you do this, I want you to… We’ve given you a lot of information now, even though it’s been four modules. But we’ve given you a lot of intake forms. Get them out. Just put the forms together, and then flip through and say, “Okay, on this patient I’m going to use this one, this one, this one, and this one.” You pull them out, and then those forms relate to that patient. And then you go through and you start checking them off. And you know that the frontal lobes coming next. You know the temporal lobe, the hippocampus is already involved. And you look at this patient, and you’re like, “I can put together a strategy of exercises, a strategy of nutrients. I know what to monitor to see if they get better, and now I monitor those things, initiate a treatment plan, and watch and see if they change,” because nothing else is changing that patient and they’re sliding downhill quick. And if you let that patient go, how much time do they probably have if they’re in stage five? Not much. Not much. Pretty soon they’ll be incapacitated, then they’ll have to be in a home, then they’ll have to have help, and you know where it goes from there. Okay?

Are you starting to see how you utilize the tools? I wanted to make sure I stopped here and I show you how to utilize the tools that we’ve given you, because most people don’t give tools like this to give you any help. It’s just a fact. Okay.

So, let’s take another look. The patient has some issues with recognizing shapes and objects. Now, this is a different issue, okay? The patient has some sensory integration issues. So if they can’t recognize shapes and objects well, versus letters and numbers, where are we talking? Right or left? Right. And geometric shapes and objects, versus words, numbers, and letters, is that parietal, frontal, or temporal lobe? It’s highly parietal. And it’s highly inferior parietal. But it’s right next to, and right below the somatosensory area, and area 5 and 7 that integrate multiple sensory issues. So this person doesn’t recognize shapes and objects well, and they don’t have good sensory integration and some sensory loss, and so you have to go back and then say this: If it’s on the right side of the brain, where’s the sensory loss? Left or right side of the body for the most part? The right side could be both, but you’ll have a predominant sense of left-sided damage, okay? So if it’s just in the median cutaneous distribution, that’s one thing. If it’s in a nerve root distribution, that’s another. If it’s parietal, it might be the whole side. Do you understand why it’s important now to check cutaneous versus dermatome versus long-tract versus the whole side, and is the face involved, and is the face on the same side or the opposite side? So when we go through sensory systems I’ll show you that.

So we know that we’re concerned about the parietal lobe. Well, what might you do for treatment? Inferior parietal lobe. We gave you this. These people can have left and right confusion, problems with math calculations, finding words left, writing left, symbols and shapes right, drawing’s right, interpreting maps. Well, here’s the cool thing. The parietal lobe integrates and changes very well, because it’s right next to the area that processes sensory input. So you give sensory input, like vibration, or like touch, or some sort of sensory stimulation, and then you start having them do the things they’re not good at, like draw a triangle and name it, and then you show them a triangle and they have to name it, or a hexagon and name it, and then they have to name the color, and then you give them several of them in a row, and then they have to recall what they were, so they use their memory. And the whole time, you’re firing up that temporal lobe with sensory input. I’ve done that with lots of patients, and at the end of the day, they’re like this: “Triangle. Square. Circle. See you later. I feel great. I’m out of here.” And you keep giving them sensory input, and give them the exercises that they just couldn’t do, and now you’ve coupled two things together to bring one area to threshold. Assuming they can metabolically handle it.


Now, the last patient I gave you, he was a metabolic nightmare. This patient was a head injury patient that happened to damage that side of their brain. It just needed to be activated. There wasn’t a lot of metabolic factors. We just needed to recollateralize and make plasticity in the parietal system. Think about how much easier it is to navigate through your life if you understand shapes, sizes, geometric figures, and you can size everything up? It’s a whole lot different.

So, there’s the findings. This is, you know, the applications. I mean, the applications you can be as creative as you want. You can have them draw things with their left hand, put it in their left visual field, which is right brain; the left hand is going to be right brain. You can do all of these things. Have them draw it, have them say it. If you say it, that’s now connecting the frontal lobe to the parietal lobe. If you have them translate towards it, or away from it, and they converge or diverge, now that’s the midbrain that’s involved, and vestibular activation. There’s so many things you can do to make this parietal lobe come to threshold, as we go further along and we teach you how to integrate multiple systems into one clinical strategy. That’s what makes this super fun. This right here is – was – very easy to change. And these people, you know, if it’s on the other side they may have some other problems. So get creative with your treatment.

Here’s another patient. This patient had a head injury. Patient has aphasia. Uh-oh, what does that mean? They don’t talk well. Now again, in the member section I broke… I just feel like we didn’t do a good job on this, so we just broke down each one step by step. So if you want to go back and watch those again, I think if you watch them once or twice, you’ll never have a problem again, because it follows a simple flow chart, and I just drew each one of those out. Instead of going through the whole thing, I just drew each leg of it out and discussed it, and then did some summarizations on each side of it, and I think it’ll help you out.

Now, let’s just see if you know the answer here. They’re not fluent. Remember, I told you: Fluency, compre-hension, and repetition are the things that are important. So the person is not fluent, they do comprehend, but they don’t repeat. I’m just going to give you about ten seconds to write down what type of aphasia you think this is. Now, this is really important, and I’ve said this from the beginning, and I kind of, like, said it, but didn’t do it right. I said that most people that understand neurology don’t know language deficits, and then I didn’t teach language deficits good enough to make people know it the way they should. So that’s why we’re going through it yet again, and we’re going to go through it again.

How many people have language deficits with cortical damage? A lot. It’s just part of their damage. They can’t ambulate well. Okay, so is speech motor output? Is it usually left or right? It’s usually left. Now, if I say that they can’t ambulate well, and has tightness on the left side of their body… Let’s strike that. Let’s say the right side of their body, okay? Sorry. Let’s say the right side of their body. Just for right now. So, if there’s a speech center, is it more in the midline or is it a little bit more anterior. It’s a little bit more anterior, but if the damage goes back a little bit further, it may have damaged not just the language centers, but it might have damaged the motor centers for that patient as well. Okay? So then you have to start thinking, “Wow. How much area got damaged during this head injury?” And they have limb weakness and disuse.

[1:49.52]

Now, when I say “weakness,” you have to say “Okay, Brandon. Is this upper or lower motor damage?” And I have to say, “It’s disuse.” They’re getting weak because they can’t use it. So when we say disuse atrophy, we typically are referring to an upper motor lesion. When we say denervated weakness, we’re referring


to a lower motor lesion. So now you have this person, they can’t talk, they’re spastic, they can’t move this side, and they got smacked on the head. Now, how many of you think this is a Wernicke’s aphasia? How many think this may be Broca’s? Okay. Interesting. So, was there an aphasia? Yeah. Were they fluent? No. How come they’re not fluent? Because the motor center is not consistently working. It’s broken. Now, could they comprehend? Yeah. But, could they repeat? No. Is this an important slide? Yes. Hopefully you would at least perceive that.

Watch again. Person comes, gets smacked in the head. Their motor systems are broken. How do we know their motor systems are broken? They’re not fluent, and they don’t move well on the other side of the body. They can comprehend, so is the back of their brain intact? So now, which area’s busted? Wernicke’s? Or Broca’s? Broca’s. Wernicke’s is back there going, “I’m getting it. I’m giving the information to anterior Broca’s, but Broca’s? You’re broken.” So, they can comprehend; they are not repeating well because they are not fluent. So you say, “Man, this guy got dinged up here, or maybe they got dinged back here and it contracouped. Whatever the case may be. I don’t care about the trauma. People try to forensically break these down all the time, and it never really works unless there’s like, bone chips and fractures and stuff. But you look at it, and you’re like, “They can’t move well,” which is right here in the motor strip, and, “They can’t speak well,” which is a little bit anterior. You see this in strokes, you can see it trauma. I told you there was trauma in this case.

Watch. You’re like, “I don’t understand the weakness pattern here, Dr. Brock.” You go, “Well, their reflexes are hyperreflexive.” There’s weakness. I told you there’s some spasticity, and there’s some disuse. So this person’s hyperreflexive, they have gait changes because they can’t move well, and they have disuse. These all relate to upper motor findings. You can just get this piece of paper, check it off, and say, “You’ve got every finding of upper motor lesion.” And from this you can say, “You’ve probably got clonus. You might have upgoing toes. You’ve got disuse. There’s no fasciculations, there’s no active denervation. This is not lower motor, this is upper motor.”

Now, as we get going, we’ll go beyond clonus, Babinski, and all that, and we’ll start saying, “What does that mean to your posture, your center of pressure, and your ability to walk? And how do you rehabilitate it?” But I have to get you to the point where you can say, “There’s trauma. This is the part of the brain that’s affected. There’s language. There’s motor output. It’s upper motor. They’re spastic. There is going to be a gait change. I watched them walk. I can name it. They have a spastic gait.” What is that eventually going to do to the rest of them plastically? When I mean plastically, I mean how is that going to affect the brain and their first, second, third order neurons from having a change of feedback from that spastic side? Notice I did not say there’s weakness with denervation and an EMG that shows the muscles dying because the nerve is dying.

So I’ve shown you, now, a chart that shows where the hippocampus is, what kind of dementia it is, how to break those down. We’ve now looked at: is it upper versus lower, how to break that down. We’ve now looked at speech, how do you break that down? Start using the charts.

Okay, so, we determined it’s central nervous system. We look at that last chart. This is why I made this one. It’s a central nervous system disorder, and it’s upper motor. You have to determine if they’re rigid or spastic now, because if they’re spastic, you know their corticospinal pathways have been damaged, and their cortex has been damaged. If I told you, “No, it’s rigid,” you would say the basal ganglia’s been damaged.


Two different areas, two different treatments, two different etiologies, two different understandings. Do you understand, if you turn left or right, at this point it makes a difference. Okay.

So, what I just did… Let me just kind of go back. I took this chart and applied it to the case, and then I took it a step further and said, “Well, it is central nervous system. It is spastic. The corticospinal system is screwed up, and that’s what creates the hyperreflexia. And that’s what creates the upper motor findings.” So I’m trying to give you the chart to you can put them all together and just check them off, and then at the end of it, you say, “Look at everything I checked off. It only points to one thing in one area, and it can only be one thing in one area.” It’s your way to learn instead of just sitting here and listening to somebody talk and hoping and praying to God that you go home and get it. Pull the charts out, print them off, start using them. Let me say it again: Pull the charts, print them, and start using them. It will be a road map to where the problem is, and then when you learn more clinically, it will help you circumnavigate the additional components to the chart that you can only get from your clinical skills.

I would have probably killed for this information when I first started, because we had no idea where to start. We had no idea where to start, we had no idea how it integrated, and I’m like, “Wow, man, I would just like to have a road map to the frontal lobe here.”

And look at this person. We know they have frontal lobe changes. We know there’s Broca’s, because they weren’t fluent, they could comprehend, but they couldn’t repeat. Broca’s. End of story. And they couldn’t move their body well, because their motor strip and their corticospinal system’s been damaged, so now they’re spastic. And now they’re hyperreflexive, and now they have disuse. And you look at this, and you say, “Wow man, they have a non-fluent speech; some speech therapy with handedness to the left side of the brain is going to be integral to this patient, along with movement of the limb to reduce the spasticity.”

And then here’s the rest of the frontal lobe. The other areas that might be damaged. The supplementary motor areas, and the motor strips. And we notice that there’s a difference in muscle tone, because they’re spastic. And here’s the exam findings. I told you, there was a Babinski, there’s clonus, there’s hyperreflexia. There’s going to be motor changes. And when we apply this, we’ve got to do motor activities that decrease flexor versus extensor tone.

On Friday nights, I’m giving at least a twenty-minute extra section on adjustments and setups. And I’m going to work through the whole body over the next four or five modules. How many of you that are in the room went to that last night and thought that was a pretty okay section? The setups are cool, man. Just showing you, like, how to stretch a muscle, how to fast-stretch a muscle, how to do things that correlate with this, so you change the gain and sensitivity of a spindle, so it doesn’t stay as spastic, and it can start to open up. As you can open up that arm and get more range of motion, the contralateral brain will recollateralize, and it’ll start to get verbalization back as their hand comes back. So for me, this person, if they’re like this, I want to get the hand open and get their fingers moving while they’re talking, because Eisner’s and Broca’s will connect, and they’ll start to get speech back with handedness. Ah, so much fun.

Okay, last patient. Couple of minutes here.

Trauma to the right arm. Humerus. Whoops. They’ve got weakness with limb extension. Okay, that’s… I should say hand or wrist extension, okay? Sensory loss over the back of the hand. You’re like, “Crap, this is


peripheral nervous system. I hate it when he does this.” Okay. The patient has normal tricep strength, but wrist drop and finger drop. The patient has good flexion.

Now, real quick. Are we talking about an individual peripheral nerve? Or are we talking about a nerve root? It’s a peripheral nerve. Okay, so what nerve might be involved here, in all this stuff down here? Remember? 6 and 7? It could be 7. But 7 will affect this and that. I’m only talking about this being affected. So what is it: 7 or radial? Radial. There’s sensory loss here. How many areas of entrapment are there? The three big nerves have three areas of entrapment. One, two, three. This down here, the supinator tunnel. The cutaneous system to the top of the hand comes off before that. But they have good tricep strength, so it’s not up here. So what’s the only place it could be in? Spiral groove. You see how easy?

[1:59.49]

So, you go through this, and I gave you this right here. Why? They have a mononeuropathy, it’s radial nerve, it’s spiral groove. That’s the lesion. So you just go through, and that’s how you walk through the road map. And then you take it a step further, and you’re like, “Here’s my individual radial nerve schematic. Let me go to it.” And you say, “Man, the only place it can be is spiral groove. And here’s why.” That’s why we made this.

Now, what could happen to this patient? Maybe they broke their humerus. Maybe they have a Saturday night palsy and they fell asleep with their arm off the bed. I don’t have any idea. Maybe somebody with a fifty-pound head fell asleep on their arm. I don’t know. But I know this: It’s not polyneuropathy. But when you look at this, it’s not that. But they do have motor findings, and they do have sensory findings, and you have to determine: is it large, small, or autonomic fibers? If they have motor findings, and you stick a needle in there and it’s actively denervating, and you get no motor units, the chances of them coming back are not as good.

Okay. I’ll show her case here in the case studies.

So, how’s that as a jog through key concepts? We went through the brain, we went through some lobes, we went through some dementias, we went through some peripheral nerves. It’s kind of a mental jog, kind of a warmup to get you going. I want you to mainly learn how to use the forms that we’ve given you. And you pull them out, and you check things off, and you check things off, and you start adding it up, and when you add it all up, it’s going to say this; it’s going to scream at you: “It’s only here. This is the only place it can be.” So pay attention, functional doctor. Everybody getting it?

Alright. Great start to the morning. We have a thirty-minute break. A thirty-minute break and we’ll start back up on vasculature.

[2:01.53]

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PeriPheral Vestibular and Cerebellum disorders with ......with aPPliCations (module Four) transcript – review of Key Concepts Presentation by drs. datis Kharrazian and brandon brock